Elephants hardly ever get cancer, but until now, researchers were stumped as to why.
In a study that could help lead to a way to wipe out the disease in people, researchers identified a cancer-destroying mechanism involving a gene that encodes for the tumor suppressor protein p53.
"We believe that p53 plays a key role in cancer suppression in mammals," said Joshua Schiffman, M.D., a pediatric oncologist at the Huntsman Cancer Institute, the University of Utah School of Medicine and the Primary Children's Hospital. Schiffman led the study appearing in the Journal of the American Medical Association.
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"Evolution had 55 million years to learn how to avoid cancer in elephants," he added, "and now we have the great opportunity to learn from this about how to treat and prevent cancer in humans, and other animals, like dogs and cats."
Before the new discovery, elephants were considered to be a walking conundrum. They have 100 times as many cells as we do, so they should be 100 times more likely to have a cell slip into a cancerous state. Yet, that's not the case. Schiffman and his team report that the cancer mortality rate in elephants is less than 5 percent, compared to 11–25 percent in people.
To investigate the mystery, Schiffman and his team collaborated with Utah's Hogle Zoo and the Ringling Bros. Center for Elephant Conservation. The scientists extracted white blood cells from elephant blood drawn during routine wellness checks. They then subjected the cells to treatments that damage DNA, a cancer trigger. In response, the p53 mediated cells committed suicide.
Further analysis found that elephants have at least 40 copies of genes that code for p53, while humans have a measly two.
"Of note, over half of all human cancers are missing functional p53, another clue to its importance in suppressing cancer," Schiffman said.
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As for why humans and certain animals, like dogs, are so cancer-prone versus elephants, he said that it is due, in part, to metabolism, reproductive strategies and lifespan. Women reproduce until their mid 40s and sometimes even into their early 50s.
"After this time, humans no longer directly pass on their genes to the next generation and the human cancer rate dramatically increases at this time until old age," Schiffman said, adding that p53 function begins a steady decline as well.
"In contrast," he added, "an elephant's size is so large, and elephants reproduce throughout most of their lifespan of over 50 years old. If elephants were not protected from cancer, the species would risk extinction because all young and non-reproductive elephants would be at such high risk to develop and succumb to cancer before they could pass on their genes."
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New approaches to treating cancer, based on p53's power, are now in the works. Schiffman and his team, for example, plan to investigate natural or synthetic compounds that can mimic the amplification of the p53-associated gene seen in elephants.
The Feld Family, owners of Feld Entertainment, Inc., the parent company of Ringling Bros. and Barnum & Bailey and the Ringling Bros. Center for Elephant Conservation, have just announced that more than $1 million will be donated to support this cancer research and to care for children suffering from the disease and other illnesses.
David Malkin, M.D., a staff oncologist and senior scientist at The Hospital for Sick Children in Toronto, says the new research presents "some intriguing observations to support a mechanism by which elephants utilize excess copies of p53" and their associated genes.
He believes that further research on elephants, and other animals that tend to ward off cancer, "may indeed provide some clues as to how we might better harness p53-regulated cellular pathways in humans."
Two other nearly cancer-free animals are the naked mole rat and the bowhead whale, which appear to use different genetic mechanisms to prevent the disease. These two animals, as well as elephants, do share a strategy of genetically killing off damaged cells.
Schiffman said, "This may be more effective of an approach to cancer prevention than trying to stop a mutated cell from dividing and not being able to completely repair itself."